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I J Bujalska
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L L Gathercole
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J W Tomlinson
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C Darimont Division of Medical Sciences, Nestle Research Center, Pfizer Global Research and Development, The Medical School, Institute of Biomedical Research, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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J Ermolieff Division of Medical Sciences, Nestle Research Center, Pfizer Global Research and Development, The Medical School, Institute of Biomedical Research, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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A N Fanjul Division of Medical Sciences, Nestle Research Center, Pfizer Global Research and Development, The Medical School, Institute of Biomedical Research, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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P A Rejto Division of Medical Sciences, Nestle Research Center, Pfizer Global Research and Development, The Medical School, Institute of Biomedical Research, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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P M Stewart
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the cell cycle ( Richon et al . 1997 ) are followed by adipogenic transcription factors, such as peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT enhancer-binding protein ( Rosen & MacDougald 2006 ). Mature adipocytes express late

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-08-0050
Volume/Issue:
Volume 197: Issue 2
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Shuang-Xia Zhao
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Shanli Tsui Department of Diabetes and Endocrinology, Department of Medicine, Ophthalmology and Visual Sciences, Internal Medicine, King's College London School of Medicine, London, UK

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Anthony Cheung
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Raymond S Douglas Department of Diabetes and Endocrinology, Department of Medicine, Ophthalmology and Visual Sciences, Internal Medicine, King's College London School of Medicine, London, UK
Department of Diabetes and Endocrinology, Department of Medicine, Ophthalmology and Visual Sciences, Internal Medicine, King's College London School of Medicine, London, UK

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Terry J Smith Department of Diabetes and Endocrinology, Department of Medicine, Ophthalmology and Visual Sciences, Internal Medicine, King's College London School of Medicine, London, UK
Department of Diabetes and Endocrinology, Department of Medicine, Ophthalmology and Visual Sciences, Internal Medicine, King's College London School of Medicine, London, UK

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J Paul Banga
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extra-ocular muscles do not express TSHR ( Paschke et al . 1993 ), but a number of other eye muscle antigens have been characterized with serum antibodies from patients with GO ( Gopinath et al . 2006 ). In addition, insulin-like growth factor receptor

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DOI:
https://doi.org/10.1530/JOE-11-0162
Volume/Issue:
Volume 210: Issue 3
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Kaitlyn A Colglazier Lilly Diabetes Center of Excellence, Indiana Biosciences Research Institute, Indianapolis, Indiana, USA

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Noyonika Mukherjee Department of Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana, USA

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Christopher J Contreras Division of Endocrinology, Department of Medicine, Roudebush VA Medical Center and Indiana University School of Medicine, Indianapolis, Indiana, USA

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Andrew T Templin Lilly Diabetes Center of Excellence, Indiana Biosciences Research Institute, Indianapolis, Indiana, USA
Department of Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana, USA
Division of Endocrinology, Department of Medicine, Roudebush VA Medical Center and Indiana University School of Medicine, Indianapolis, Indiana, USA
Center for Diabetes and Metabolic Diseases, Indiana University School of Medicine, Indianapolis, Indiana, USA

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lipid peroxidation and elicit β-cell loss in C57BL/6 mice, and these effects were associated with downregulation of GPX4 and NRF2, a transcription factor that regulates expression of antioxidant genes ( Markelic et al. 2023 ). Treatment with Fer-1 was

Article Type:
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DOI:
https://doi.org/10.1530/JOE-23-0378
Volume/Issue:
Volume 262: Issue 2
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Laura L Gathercole Oxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, UK
Department of Biological and Medical Sciences, Oxford Brookes University, Oxford, UK

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Nikolaos Nikolaou Oxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, UK

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Shelley E Harris Oxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, UK

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Anastasia Arvaniti Oxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, UK
Department of Biological and Medical Sciences, Oxford Brookes University, Oxford, UK

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Toryn M Poolman Oxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, UK

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Jonathan M Hazlehurst Oxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, UK
Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK

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Denise V Kratschmar Swiss Centre for Applied Human Toxicology and Division of Molecular and Systems Toxicology, Department of Pharmaceutical Sciences, University of Basel, Basel, Switzerland

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Marijana Todorčević Oxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, UK

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Ahmad Moolla Oxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, UK

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Niall Dempster Oxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, UK

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Ryan C Pink Department of Biological and Medical Sciences, Oxford Brookes University, Oxford, UK

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Michael F Saikali Department of Pharmaceutical Sciences, Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, Ontario, Canada

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Liz Bentley Mammalian Genetics Unit, Medical Research Council Harwell, Oxford, UK

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Trevor M Penning Center of Excellence in Environmental Toxicology, Department of Systems Pharmacology & Translational Therapeutics, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA

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Claes Ohlsson Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden

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Carolyn L Cummins Department of Pharmaceutical Sciences, Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, Ontario, Canada

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Matti Poutanen Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
Institute of Biomedicine, Research Centre for Integrative Physiology and Pharmacology, University of Turku, Turku, Finland

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Alex Odermatt Swiss Centre for Applied Human Toxicology and Division of Molecular and Systems Toxicology, Department of Pharmaceutical Sciences, University of Basel, Basel, Switzerland

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Roger D Cox Mammalian Genetics Unit, Medical Research Council Harwell, Oxford, UK

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Jeremy W Tomlinson Oxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, UK

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-0280 . Table 1 Top 10 upstream regulators in Akr1d1 –/– liver predicted by ingenuity pathway analysis (IPA). IPA of liver RNA-Seq identified core metabolic transcription factors as upstream regulators of the hepatic response to Akr1d1 deletion. In

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-21-0280
Volume/Issue:
Volume 253: Issue 3
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Gulizar Issa Ameen Department of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK

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Silvia Mora Department of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK

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factors that bind ERE sequences as homo or heterodimers. ERs contain two transcription activation functions: AF1 located in the N-terminal A/B domain and the AF2 located in the C terminal domain. AF2 is activated through ligand (hormone) binding, whereas

Article Type:
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DOI:
https://doi.org/10.1530/JOE-17-0359
Volume/Issue:
Volume 236: Issue 1
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Renata Risi Department of Experimental Medicine, Sapienza University of Rome, Sapienza University of Rome, Rome, Italy
University of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Cambridge, UK

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Antonio Vidal-Puig University of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Cambridge, UK
Cambridge University Nanjing Centre of Technology and Innovation, Nanjing, P. R. China
Centro de Investigacion Principe Felipe, Valencia, Spain

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Guillaume Bidault University of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Cambridge, UK

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Science 121 2308 – 2318 . ( https://doi.org/10.1242/jcs.026062 ) Dai C Kayton NS Shostak A Poffenberger G Cyphert HA Aramandla R Thompson C Papagiannis IG Emfinger C Shiota M , et al. 2016 Stress-impaired transcription factor

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https://doi.org/10.1530/JOE-23-0313
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Volume 262: Issue 1
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Katie J Mylonas University/BHF Centre for Cardiovascular Science, University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, UK

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Neil A Turner Division of Cardiovascular & Diabetes Research, Leeds Institute of Cardiovascular & Metabolic Medicine (LICAMM), School of Medicine, University of Leeds, Leeds, UK

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Sumia A Bageghni Division of Cardiovascular & Diabetes Research, Leeds Institute of Cardiovascular & Metabolic Medicine (LICAMM), School of Medicine, University of Leeds, Leeds, UK

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Christopher J Kenyon University/BHF Centre for Cardiovascular Science, University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, UK

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Christopher I White University/BHF Centre for Cardiovascular Science, University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, UK

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Kieran McGregor University/BHF Centre for Cardiovascular Science, University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, UK

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Robert A Kimmitt University/BHF Centre for Cardiovascular Science, University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, UK

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Richard Sulston University/BHF Centre for Cardiovascular Science, University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, UK

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Valerie Kelly University/BHF Centre for Cardiovascular Science, University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, UK

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Brian R Walker University/BHF Centre for Cardiovascular Science, University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, UK

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Karen E Porter Division of Cardiovascular & Diabetes Research, Leeds Institute of Cardiovascular & Metabolic Medicine (LICAMM), School of Medicine, University of Leeds, Leeds, UK

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Karen E Chapman University/BHF Centre for Cardiovascular Science, University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, UK

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Gillian A Gray University/BHF Centre for Cardiovascular Science, University of Edinburgh, Queen’s Medical Research Institute, Edinburgh, UK

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-differentiation factor-15 (GDF-15) as a novel inhibitor of neutrophil recruitment post MI ( Kempf et al . 2011 ). Regulation of the expression of these key molecules is a potential additional mechanism through which glucocorticoid, generated in myocardial cells by 11β

Article Type:
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https://doi.org/10.1530/JOE-16-0501
Volume/Issue:
Volume 233: Issue 3
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Bernard Freudenthal Molecular Endocrinology Laboratory, Department of Medicine, Imperial College London, London, UK

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John Logan Molecular Endocrinology Laboratory, Department of Medicine, Imperial College London, London, UK

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Sanger Institute Mouse Pipelines Mouse Pipelines, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, UK

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Peter I Croucher Garvan Institute of Medical Research, Sydney, New South Wales, Australia

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Graham R Williams Molecular Endocrinology Laboratory, Department of Medicine, Imperial College London, London, UK

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J H Duncan Bassett Molecular Endocrinology Laboratory, Department of Medicine, Imperial College London, London, UK

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al . 2009 ). The most important risk factors for osteoporotic fracture are low bone mineral density (BMD) (clinically assessed by dual-energy X-ray absorptiometry (DEXA or DXA)), increasing age and history of fracture ( Johnell et al . 2005

Article Type:
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https://doi.org/10.1530/JOE-16-0258
Volume/Issue:
Volume 231: Issue 1
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Md Nurul Islam Division of Neurology, Respirology, Endocrinology and Metabolism, Department of Internal Medicine, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan

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Yuichiro Mita Division of Neurology, Respirology, Endocrinology and Metabolism, Department of Internal Medicine, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan
Systems Life Sciences Laboratory, Department of Medical Life Systems, Faculty of Life and Medical Sciences, Doshisha University, Kyoto, Japan

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Keisuke Maruyama Division of Neurology, Respirology, Endocrinology and Metabolism, Department of Internal Medicine, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan

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Ryota Tanida Division of Neurology, Respirology, Endocrinology and Metabolism, Department of Internal Medicine, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan
Department of Sports and Fitness, Faculty of Wellness, Shigakkan University, Aichi, Japan

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Weidong Zhang Division of Neurology, Respirology, Endocrinology and Metabolism, Department of Internal Medicine, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan

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Hideyuki Sakoda Division of Neurology, Respirology, Endocrinology and Metabolism, Department of Internal Medicine, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan

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Masamitsu Nakazato Division of Neurology, Respirology, Endocrinology and Metabolism, Department of Internal Medicine, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan
CREST (Japan) Agency for Medical Research and Development (A-MED) 1-7-1 Otemachi, Tokyo, Japan

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finding in Hepa 1-6 cells. Phosphorylated AMPK suppresses the activity of sterol regulatory element-binding protein 1 (SREBP1), a key transcription factor involved in the regulation of lipid metabolism ( Li et al. 2011 ). The binding consensus sequence

Article Type:
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DOI:
https://doi.org/10.1530/JOE-19-0102
Volume/Issue:
Volume 244: Issue 1
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Dawn E W Livingstone Endocrinology Unit, Queen's Medical Research Institute, Centre for Cardiovascular Science, University of Edinburgh, 47, Little France Crescent, Edinburgh EH16 4TJ, UK

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Sarah L Grassick Endocrinology Unit, Queen's Medical Research Institute, Centre for Cardiovascular Science, University of Edinburgh, 47, Little France Crescent, Edinburgh EH16 4TJ, UK

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Gillian L Currie Endocrinology Unit, Queen's Medical Research Institute, Centre for Cardiovascular Science, University of Edinburgh, 47, Little France Crescent, Edinburgh EH16 4TJ, UK

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Brian R Walker Endocrinology Unit, Queen's Medical Research Institute, Centre for Cardiovascular Science, University of Edinburgh, 47, Little France Crescent, Edinburgh EH16 4TJ, UK

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Ruth Andrew Endocrinology Unit, Queen's Medical Research Institute, Centre for Cardiovascular Science, University of Edinburgh, 47, Little France Crescent, Edinburgh EH16 4TJ, UK

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the QuantiTect DNase/reverse transcription kit (Qiagen Ltd). cDNA (equivalent to 10 ng total RNA) was incubated in triplicate with 1× gene specific assay mix (Applied Biosystems, Warrington, UK) in 1× LightCycler480 Probes mastermix (Roche Diagnostics

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-09-0003
Volume/Issue:
Volume 201: Issue 2
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